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,2
* FG Tierhaltung und Leistungsphysiologie, Institut Tierhaltung und Tierzüchtung and
and
Landesanstalt für Landwirtschaftliche Chemie, Universität Hohenheim, 70599 Stuttgart, Germany
2 Correspondence:
Garbenstr. 17 (phone: 0049/711/459-2455; fax: 0049/711/459-2498; E-mail:
thsekret{at}uni-hohenheim.de).
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Abstract |
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Two groups of six barrows were provided with catheters in the jugular vein and fed either a ration with pregelatinized starch (high ileal digestibility; controls) or potato starch (low ileal digestibility; PS) as the main carbohydrate. All pigs were fed 31 MJ of metabolizable energy and 381 g of crude protein per day. The controls were fed for 19 d. The PS group received the same control ration for 10 d, and then changed to the PS ration. The total feeding period of PS consisted of a 5-d adaptation period followed by another 19 d. In the continously sampled feces, pH, short chain fatty acids, and skatole were determined. Skatole was additionally measured in blood plasma that was sampled daily. After killing barrows at the end of the feeding period, fat tissue for skatole measurement and colon tissue for histological quantification of mitosis and apoptosis were obtained. Feeding potato starch led to a rapid 2.2-fold increase of fecal butyrate when compared both with the control period of the PS group and the control group (P < 0.001). PS feeding resulted in a decrease in pH from 7.3 to 5.3 (P < 0.001) and apoptosis from 2.06 cells/crypt to 0.90 cells (P < 0.01), whereas there was no change in mitosis. Consequently, skatole decreased both in feces (controls vs PS group: 120.0 vs 1.9 µg/g; P < 0.001) and in blood plasma (1.6 vs 0.2 ng/mL; P < 0.001). The mean concentration of skatole in fat tissue was 167 ng/g tissue in controls, and below the detection limit (0.8 ng/g) in the PS group (P < 0.001). It is concluded that butyrate-dependent inhibition of apoptosis in the colon due to potato starch feeding efficiently inhibits skatole production in barrows. Because of the depressed skatole levels, improved sensory quality of pork is possible.
Key Words: Apoptosis • Butyrates • Colon • Pigs • Potato Starch • Skatole
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Introduction |
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The supplementation of pig rations with tryptophan did not increase skatole formation (Mortensen, 1989; Bernal-Barragan, 1992), probably because this amino acid is absorbed in the small intestine. Alternatively, cell debris resulting from apoptosis of intestinal mucosa cells is a substrate for skatole formation (Claus et al., 1996). Because apoptosis is linked to the regulation of intestinal cell renewal, and thus to the anabolic hormones, these mechanisms can provide an explanation for sex differences in skatole formation (Claus et al., 1994). Increased energy supply led to a rise in IGF-1 concentrations in blood plasma. The concomitant increase of the mitotic and apoptotic index in the gut mucosa explained an energy-dependent increase of skatole under experimental and routine fattening conditions (Neupert et al. 1995; Claus et al., 1996; Raab et al., 1998). Some cell debris from apoptosis in the small intestine is reutilized before entering the large intestine, and therefore, it is possible that apoptosis in the colon is more important for skatole formation. Recent studies demonstrate that apoptosis in the intestine is inhibited by butyrate (Hass et al., 1997; Mentschel et al., 2001). Resistant potato starch is known to increase mainly butyrate formation in the colon (Martin et al., 1998; Govers et al., 1999; Topping and Clifton, 2001). The objective, therefore, was to test the hypothesis that apoptosis in the colon of pigs could be reduced by feeding a ration with a high potato starch (PS) content leading to decreased skatole formation, as well as reduced absorption and accumulation of skatole in adipose tissue.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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Elevated skatole concentrations, which exceed 200 ng/g fat, are usually found in less than 10% of boars and only occasionally in barrows and gilts. Therefore, it is very difficult to set up uniform experimental groups with high skatole concentrations. Luminal nutrient availability influences the expression of IGF-I messenger RNA and its receptor in the intestinal tract. Glucose is known to be the most potent stimulator of IGF-I (Ziegler et al., 1995; MacDonald, 1999; Wang et al., 2000). Therefore, we intended to feed two experimental groups of barrows for 10 d with gelatinized starch. This type of starch is easily digested in the intestinal tract and thus has a high potential to stimulate IGF-I expression in the tissue. An increase in mitosis and apoptosis should follow, leading to an elevated skatole formation out of the apoptotic cells. After this period, the apoptosis should be decreased in one of the groups by feeding PS for 19 d. Potato starch is a resistant starch that is metabolized to short-chain fatty acids (SCFA), preferentially butyrate, in the colon. The other group should be further fed with gelatinized starch for a total of 19 d (control). Therefore, the feeding period for the two types of starch is identical, but the barrows of the PS group would be older due to the preconditioning period. So far, no systematic effect of the age at slaughter on skatole concentrations could be detected (Neupert et al., 1995; Weiler et al., 1995; Moss et al., 1997). Instead, the prolongation of the gelatinized starch-feeding period in the control group would probably continuously raise the mitotic levels above those in the PS group, making it impossible to differentiate a specific role of apoptosis inhibition.
Animals and Feeding Regime
Twelve German Landrace x Pietrain barrows were kept in individual crates (3 x 2.5 m) without straw. At an average weight of 60 kg (range: 55 to 65 kg), the barrows were fitted with indwelling jugular vein catheters, as described by Claus et al. (1990). The cannulations had been approved by the local animal welfare committee and were performed under a surgical plane of general anesthesia. The catheters were inserted into the cephalic vein and were pushed forward until the catheter tip was located in the jugular vein close to the heart. After surgery, the pigs received an intramuscular injection of antibiotic (Veracin, Albrecht, Aulendorf, Germany), but no antibiotics were fed during the following experimental period.
The feeding experiments started about 1 wk after surgery when the pigs had completely recovered. They were allocated to the two feeding groups (for details of the rations and the nutrient supply, see Table 1
). Both experimental groups were fed the ration with pregelatinized starch as the main energy source. The energy content was 14.13 MJ ME/kg DM, and the crude protein content was 174 g/kg DM. The groups were fed 2.19 kg/d of diet twice daily for 10d, for a total of 31 MJ of ME and 381 g of crude protein per day. The control group was fed with the gelatinized starch ration for another 9 d, resulting in a total experimental time of 19 d.
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). Based on the estimated losses by bacterial fermentation (Kirchgessner, 1997), the calculated energy content was only 12.46 MJ ME/kg DM, and the crude protein content was 153 g/kg DM. This loss was compensated for by increasing the daily supply of feed up to 2.49 kg/d so that both groups received the same amount of energy and protein. This ration (Table 1) was also fed twice daily. According to Topping et al. (1997), the first 5 d were taken as an "adaptation period," followed by another 19 d of the PS diet. Consequently, both groups were under the influence of the corresponding types of starch for 19 d. Because it is known that the intestinal transit time is about 1 d (Ehle et al., 1982), the first day with the experimental control diet was omitted from the evaluation. All pigs had free access to water. The resistant starch content of raw potato was additionally verified by an in vitro digestion analysis, as described by Faisant et al. (1995) and Morales et al. (1997). The content of resistant starch in the raw PS was 80%, as was reported by Morales et al. (1997).
Sample Collection
Blood samples for determination of skatole were obtained by catheter twice daily at 1000 and 1700. The catheters were rinsed carefully with sterile heparinized saline after each sampling. Before sampling, a volume of 5 mL was discarded. Blood was collected in heparinized vials, centrifuged, and the plasma was stored at -22°C until assayed for skatole concentration. Only the morning samples were used for analytical evaluation.
Fresh feces were collected every morning, and a quantity was used for pH determination. Portions were also deep-frozen (-22°C) until determination of skatole and SCFA.
At the end of the feeding periods, the pigs were killed by intravenous infusion of 20 to 30 mL of Narcodorm-n (Alvetra, Neumünster, Germany). Tissue samples were taken within 5 min from three sites on both the proximal and distal colon. They were immediately rinsed with cold physiological saline and fixed overnight in 4% paraformaldehyde. They were then dehydrated in a graded series of ethanol and embedded in paraffin for later immunocytochemical analysis of mitosis and apoptosis. Adipose tissue samples were taken from back, ventral, and abdominal fat. They also were deep-frozen at -22°C until measurement of skatole.
Skatole Determination
Skatole in blood plasma was determined as described earlier (Claus et al., 1993). In brief, a diethylether extract of plasma was evaporated after addition of the HPLC eluent and chromatographed by reverse-phase–HPLC with fluorescence detection. The chromatographic conditions were as follows: column, 250 x 4 mm Grom-Sil ODS (particle size: 5 µm; Grom, Herrenberg, Germany); eluent, 0.02 M acetic acid:acetonitrile:2-propanol (55:30:15 vol/vol/vol); flow, 1.0 mL/min; wavelengths, Ex 275 nm, Em 352 nm. The lower limit of sensitivity was 0.06 ng/mL of plasma.
Skatole in adipose tissue was determined as described by Dehnhard et al. (1993). Melted fat was dissolved in n-hexane and extracted with acetonitrile:water (3:1 vol/vol). The extract was chromatographed on HPLC with the same conditions as described for skatole determination in plasma. The emission wavelength of the fluorescence detector was set to 345 nm. The lower limit of sensitivity was 0.8 ng/g fat.
Skatole in feces was also determined by reverse-phase–HPLC (Dehnhard et al., 1991). Samples were extracted with methanol and purified on Amberlite XAD-7. Dried residues from methanol-extracted feces were taken for DM determination as a basis for skatole and SCFA contents in feces. The chromatographic conditions were the same as described above. The detection wavelength was 280 nm. The lower limit of detection was 0.4 µg/g of dry feces.
pH Determination
The pH was determined according to Topping et al. (1993) by diluting 0.5 g of feces with four weight volumes of water. Samples were centrifuged (3,000 x g, 15 min, 20°C) and the pH was measured by pH electrode.
Determination of Short-Chain Fatty Acids
Short-chain fatty acids (acetate, propionate, and butyrate) in feces were determined in duplicate. The samples (0.4 g) were brought up to a mass of 0.5 g with distilled water, vortexed after adding 2.5 mL of 0.25 M sulfuric acid, and centrifuged (3,000 x g, 5 min). A 1.4-mL sample of the supernatant was transferred to a tube and centrifuged at 14,000 x g for 10 min. Of the resulting supernatant, 900-µL was mixed with 100 µL of 19.6 µmol/mL of 2-methylvaleric acid (internal standard for gas chromatography). For calibration, aqueous standard solutions were used. The concentrations for these solutions ranged between 1.25 and 80 µmol/mL (acetate), 0.63 to 40 µmol/mL (propionate), and 0.31 to 20 µmol/mL (butyrate). Results were standardized to the dry weight of feces.
The gas chromatographic analysis was performed as described by Tangerman and Nagengast (1996). The system consisted out of a GC 8000 (Fisons, Milano, Italy) connected to a flame ionization detector EL 980 (Fisons) and an A200 S automatic liquid sampler (CTC Analytics, Zwingen, Switzerland) with an injection volume of 1 µL. The glass liner of the injector was filled with small glass beads (60/80 mesh, Alltech, Deerfield, IL) and plugged with glass wool. The needle of the autosampler syringe penetrated these glass beads by about 1 cm. For reproducible results, the injector was primed by the injection of approximately 30 feces samples. Ghosting was prevented by the injection of 1 µL of 10% formic acid after two chromatographic runs. Other chromatographic conditions were as follows: column, 30 m x 0.25 mm BP21 with 0.25-µm film thickness (SGE, Weiterstadt, Germany); injection port temperature, 170°C; detector temperature, 220°C; carrier gas was He, 100 kPa; H2, 70 kPa; air, 100 kPa; column temperature program, 100°C (1 min), 200°C (20°C/min), 200°C (2 min).
The accuracy was determined by adding known amounts of SCFA to a fecal sample with endogenous amounts of 24.9, 9.0, and 4.5 µmol/g DM for acetate, propionate, and butyrate, respectively. The spiking amounts of SCFA added were 10 and 20 µmol/g DM for acetate, 5 and 10 µm/g DM for propionate, and 2.5 and 5 µmol/g DM for butyrate (n = 3). Repeatability was determined by repeated measurement of a sample on the same day (intraassay repeatability, n = 16) or on consecutive days (interassay repeatability, n = 10). The sensitivity was defined as threefold the background reading of the detector.
Immunocytochemical Evaluation
To characterize mitosis, sections of 2 to 3 µm were deparaffinized, rehydrated, and stained using histoprime monoclonal antibody (Ki 67 MIB-1; Canon, Wiesbaden, Germany). Details of the staining procedure were described earlier (Mentschel et al., 2001). Nonspecific background was reduced by incubation with normal horse serum diluted 1:10. Endogenous peroxidase was blocked by incubation in 3% H2O2. Counterstaining was performed by hematoxylin-eosin (Merck, Darmstadt, Germany).
Cells undergoing apoptosis were identified by a modified terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick-end labeling (TUNEL) assay (Gavrieli et al., 1992) that leads to a staining of apoptosis-specific DNA fragments. The staining reaction was based on the in situ cell death detection kit POD (Boehringer, Mannheim, Germany). Details of the procedure were described elsewhere (Mentschel et al., 2001). Negative controls were treated the same way as the normal slides, but the enzyme solution in the TUNEL reaction mixture was omitted. Again, hematoxylin-eosin was chosen for counterstaining.
The immunocytochemical evaluation was confined to those crypts where the entire length could be evaluated. Thus, in each of the three sections representing the three sampling sites from the two colon compartments (proximal and distal), 30 to 40 crypts were evaluated. The total cell number per crypt was used to characterize the crypt height. The apoptotic activity is given as the total number of TUNEL-positive cells per crypt. To characterize the location of apoptotic cells, they were allocated to one of four equal compartments along the longitudinal axis.
For mitosis evaluation, the Ki-67–positive cells were related to the total number of epithelial cells along the hemicrypts. The ratio between the labeled and total cells was expressed as percentage and taken as a mitotic index. The total cell count was used separately to characterize the height of the crypts.
Statistical Analysis
The effectiveness of PS to decrease skatole formation was characterized by comparing the tissue concentrations of skatole in the controls and in the PS barrows. In addition, the differences in blood and feces parameters before and after the change of the ration were compared within the feeding groups.
The data are presented as group means ±SEM and were tested for normal distribution by the Kolmogorov-Smirnov test. For continuous data (skatole, SCFA, and pH), differences between both groups (control vs PS) were analyzed by independent-sample t-test. Differences between treatment periods within one group were evaluated by paired-samples t-test. Both tests were evaluated using daily values of each individual. Data from the adaptation period were omitted because continuously increasing or decreasing values within this 5-d period were observed. The correlations between skatole concentration in plasma and feces were determined by Spearman’s rank correlation (nonparametric method). They were based on the daily data of each individual, including the adaptation period. Immunocytochemical data (apoptosis and mitosis) were processed as follows:
For each animal and parameter, the mean value was calculated in each region, from at least 30 crypts. These data were analyzed as a split-plot design using the mixed model analysis of the Statistical Package for the Social Sciences (version 11, SPSS, Chicago, IL). The following model was used:
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where Yijk = mean count at jth position on kth animal within ith group; µ = general effect; ai = main effect of ith group; ßj = main effect of jth position (region); fik = effect of kth animal within the ith group; (aß)ij = group x position (region) interaction; eijk = residual error. In this design, the animal effect was specified on RANDOM.
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Results |
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The sensitivity of the method was 0.5 µmol/g DM. The recoveries of the SCFA from spiked samples with low levels were 82%, 79%, and 80% for acetate, propionate, and butyrate, respectively. For high levels, they were 85%, 83%, and 83% for acetate, propionate, and butyrate, respectively. Determination of repeatability data revealed intraassay coefficients of variation of 3.7%, 2.4%, and 2.0% for acetate, propionate, and butyrate, respectively, and interassay coefficients of variation of 13.1%, 7.6%, and 11.5% for acetate, propionate, and butyrate, respectively.
Short-Chain Fatty Acids in Feces
The changes in SCFA over time are given in Figure 1 for both the controls and the PS group. In the controls, acetate was the predominant acid present in feces, with an average level of 190 ± 6.22 µmol/g DM. The concentrations revealed a random day-to-day variation, but no systematic change from the mean during the whole experimental period. Both propionate and butyrate had a similar range of concentrations (67 ± 2.55 µmol/g DM for propionate, and 65 ± 3.85 µmol/g DM for butyrate, respectively). The latter acid increased during the first 4 d of the feeding period and then reached a plateau around the mean value (72 ± 3.15 µmol/g DM).
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When compared to the reference period, feeding of PS led to a 1.6-fold increase of acetate (P < 0.001) and an even more pronounced increase for butyrate (2.2-fold; P < 0.001). Propionate, in contrast, was not significantly altered (0.95-fold).
pH Values
Changes in pH overtime are given for the two groups in Figure 2. As expected, the pH did not change noticeably in the controls. The mean pH was 7.36 ± 0.04 over the entire feeding period. A similar mean pH was measured during the reference period of the PS group (7.31 ± 0.06). During PS feeding, pH decreased to 5.26 ± 0.05 during the 5-d adaptation period and remained close to this level for the rest of the feeding period (P < 0.001).
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Histological examination revealed that mitotic activity was mainly concentrated in the base compartments of colonic crypts for both groups. The quantitative results for the mitotic and apoptotic activity in the colon of the two groups are summarized in Table 2. For mitotic evaluation, no significant effect could be calculated (main effects or interactions). There were no significant differences in mitotic activity between the two feeding groups. In contrast, diet had a strong effect (P < 0.01) on apoptosis in the colon, whereas apoptosis in the proximal and distal colon did not differ significantly (P = 0.076). There was no group x region interaction (P = 0.385).
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Skatole in Feces, Blood Plasma, and Fat
In feces (see Figure 3), the mean skatole concentration in the controls was 70 ± 5.44 µg/g DM during the first 4 d and increased thereafter up to a plateau of 127 ± 13.81 µg/g DM. In the reference period of the PS group, the mean skatole concentration was 99 ± 3.39 µg/g DM. After switching to the PS diet, the concentrations decreased abruptly during the 5-d adaptation period to minimal concentrations, which were partly below the detection limit in some individual pigs. This minimal level was reached by the fourth day after feeding PS. Thereafter, the skatole concentrations remained at a low level of only 1.87 ± 0.23 µg/g DM, which was only slightly above the sensitivity of the assay (0.4 µg/g).
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), the overall agreement between the two patterns is obvious. In the controls, the blood plasma values showed increases parallel to those found in feces. The correlation coefficient among skatole concentrations in blood and feces was r = 0.93 (P < 0.001). The mean blood plasma concentration of skatole in controls was 1.51 ± 0.09 ng/mL.
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The resulting fat tissue concentrations of skatole in the controls were highest in abdominal fat (236 ± 31 ng/g; range 136 to 384), intermediate in ventral fat (159 ± 26 ng/g; range 73 to 302), and lowest in backfat (113 ± 16 ng/g; range 47 to 149). Altogether, three out of the six pigs revealed concentrations above 250 ng/g in at least one compartment. In the PS animals, all skatole values in adipose tissue were below the assay detection limit (0.8 ng/g fat).
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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The results of this study show that feeding resistant PS to the high skatole-producing barrows led to an increased formation of SCFA in the colon. Acetate was still the predominant fatty acid, but the increase of butyrate in pigs was even more pronounced. Butyrate has been shown to specifically inhibit apoptosis and thus may reduce the availability of cell debris for microbial formation of skatole. The result is expected to lead to a dramatic decrease in skatole formation and accumulation in carcass tissue. The results of the current study support the hypothesis that fermentation of endogenous epithelial residues in the colon contributes substantially to skatole formation.
Two main theories have been offered to explain the sex-dependent and individual variation in the carcass fat skatole concentration in pigs. One theory assumes that an increased hepatic metabolism of skatole after absorption from the colon leads to low tissue concentrations. The other theory assumes that skatole formation in the colon ultimately determines tissue concentrations and levels can be influenced by feeding. Several studies were performed to relate tissue concentrations of skatole to the oxidizing and conjugating activity of liver enzymes, such as unspecific pyrrolooxygenases (Frydman et al., 1972) or cytochrome P450 II E1 (Babol et al., 1998a; Baek et al., 1998). The effect of this cytochrome, however, was most likely overestimated because the rate of skatole metabolism in the liver in vitro was not related to skatole clearance and deposition in fat. Nevertheless, metabolic biotransformation of skatole in the liver may have an effect on skatole levels in fat (Babol et al., 1998b).
Therefore, variations in the microbial formation of skatole due to feeding influences are more likely to explain differences in tissue concentrations. Such an assumption is supported by several studies that demonstrate a significant correlation between concentrations in feces, peripheral blood plasma, and adipose tissue (Herzog et al., 1993; Claus et al., 1993; Herzog, 1994). In the present study, under standardized experimental conditions, the skatole profiles in feces and blood plasma revealed the same pattern and thus were highly correlated. The results contrast with studies where only a slight tendency towards a relationship between the concentrations measured in the feces and in plasma was detected (Jensen and Jensen, 1998). The discrepancy between studies and an explanation for the less pronounced influence of liver enzymes may be due to the fact that skatole is mainly formed in the rectum (Bernal-Barragan, 1992). It was shown by measurements in blood collected from the vena cava that high amounts of skatole are absorbed from the rectum and thus are delivered to peripheral plasma without a passage through the liver (Claus et al., 1993). Minor influences on the location of skatole formation and absorption within the large intestine include factors such as variation in intestinal transit time. Such a prolongation in the transit time would increase the time for microbial degradation of tryptophan and explain the high correlation between the concentration of skatole in feces and the DM content of feces (H. Bernal-Barragan, R. Claus, and A. Herzog; unpublished observations).
Several in vivo and in vitro investigations were performed to detect effects of feed components on skatole formation. Increasing the pH in the gut by feeding sodium bicarbonate (Claus et al., 1994) led to an elevation in fecal pH and a decrease of skatole in adipose tissue by 40%. Such an effect of the pH is explained by the fact that a rising pH favors a microbial degradation of tryptophan to indole instead of skatole (Jensen and Jensen, 1998). Based on the latter argument, the low pH in the PS group should have favored higher blood plasma concentrations. This was not the case in the present study. Collectively, the data support the assumption that the degree of mucosal cell debris likely plays a key role for skatole formation.
Studies on the consequences of different diets for skatole formation revealed that high contents of carbohydrates with a low ileal digestibility tend to decrease skatole (e.g., Hawe et al., 1992; van Oeckel et al., 1997). A few in vivo and in vitro studies compared influences of different fiber types on skatole formation and absorption and found an effect for fructooligosacharides and PS (Jensen and Jensen, 1998). Fructooligosaccharides had also been shown earlier to decrease skatole in adipose tissue (Claus et al., 1994). So far, however, the physiological mechanisms of these effects were not clarified.
We favor the assumption that shedded cells from epithelial cell turnover in the gut are the main substrate for proteolysis and tryptophan fermentation in the colon (Smith and Macfarlane, 1996). Thus, any dietary composition that influences the regulation of the mitosis–apoptosis equilibrium in the epithelia might have an effect on skatole formation. An elevation of the energy content in the ration led to a rise of mitosis, but also a counteracting apoptosis in the small intestine. This effect was shown to be mediated via growth factors such as IGF-1 (Raab et al., 1998). Additionally, purines increased mitosis and later cell death. Both stimuli led to clearly elevated skatole concentrations in blood plasma (Claus et al., 1996; Raab et al., 1998). In the present study, an attempt to decrease skatole formation via butyrate was successful. The limited availability of cell debris for the microbes is partly explained by the decrease of the apoptotic rate. In addition, the remaining apoptosis was shifted toward the proliferative compartment. It is known that cells undergoing apoptosis in that part of the crypt are eliminated mainly by engulfment by adjacent cells, especially neighboring macrophages (Kerr et al., 1994; Sträter et al., 1995), a response that would further restrict the amount of cell debris in the lumen. The antiapoptotic effect of butyrate seems to contradict the apoptosis-accelerating effect discussed for human medicine. This latter effect, however, was mainly supported by in vitro studies and appears to be limited to transformed tumor cells (Heerdt et al., 1994). Under in vivo conditions and in nontransformed cells, an antiapoptotic effect was demonstrated for the guinea pig colon (Hass et al., 1997). The same response was seen in the bovine rumen by directly feeding SCFA (Mentschel et al., 2001).
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Footnotes |
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Received for publication December 7, 2001. Accepted for publication August 19, 2002.
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